The risk of transmission of prions during dental care is not known,
although on existing evidence it is likely to be very low. Although prions may
be detected in the oral tissues of inoculated laboratory animals, at present
there are no published reports of the detection of prions in nonlymphoid
tissues of humans with any form of Creutzfeldt—Jakob disease (CJD). The
present article reviews current knowledge of the presence of prions in the
mouth, discusses the possible transmission of prions via oral tissues and
outlines the possible modifications of infection control measures required for
the dental health care of patients with prion disease.

PRIONS IN THE DENTAL HEALTH CARE SETTING

Transmission of sporadic CJD by dental treatment was proposed as long as 20
years ago1,
2. Later, reporting three
patients in Japan with sporadic CJD, Arakawa et
al.3 suggested
that prions might have been acquired as a consequence of dental treatment but
did not provide any supporting data. Case—control studies have never
revealed any association between dental health care and the development of
either sporadic4 or
iatrogenic5 CJD, and
at present there are no data to suggest any clustering of variant CJD (vCJD)
about a dental practice.

Prions in oral tissues

Prions have been detected in the oral and dental tissues of animals with
experimental scrapie, and the finding of neuronal degeneration with probable
prion protein accumulation in the trigeminal ganglia of patients with sporadic
CJD points to a possible route of transmission of prion from the brain to the
oral tissues (and vice
versa)6.
Inoculation of scrapie agent into the peritoneum or dental pulps of hamsters
leads to eventual prion infection of the trigeminal ganglion on the side of
inoculation7, the
estimated rate of travel along the trigeminal nerve being 1 mm per day.

Prion protein was not detected in the pulpal homogenates of 8 US patients
with sporadic CJD8;
however, intraperitoneal injection of scrapie agent led to infection of the
dental pulps of hamsters after about 96
days7. Prions were
also detected in the gingival tissues of these animals after about 760 days,
the concentration of prion being higher in gingival than in pulpal tissue.

Since prion protein of vCJD is present in tonsillar lymphoid
tissue9 it is likely
to be present also in lingual tonsil. In addition, the tendency for prion of
vCJD to occur at sites outside the central nervous system suggests that it
will be present in the trigeminal ganglion—particularly since the prion
of bovine spongiform encephalopathy (BSE) can be present in peripheral
nerves10.

Infectivity

There is no definitive evidence that prion disease can be transmitted by
oral tissue, although biting is a possible explanation for accidental
transmission of scrapie between encaged
animals11. Gingival
scarification with burrs previously used to scarify scrapie-infected mice did
not lead to
scrapie1, although
intraperitoneal injection of gingival tissue did give rise to astrocytosis of
scrapie in mice. Also, gingival exposure to scrapie-infected brain homogenate
caused scrapie in recipient
mice12. Of note,
while gingival scarification (e.g. with forceps and scissors) caused
transmission to all laboratory animals, disease also developed in 71% of
animals gingivally exposed to brain homogenate but not scarified. Early
studies suggested that gingival extracts have low
infectivity1,
12—for example,
intracerebral inoculation of gingival tissue from scrapie-infected mice only
caused scrapie in 3 of 31
mice12—but
later work revealed substantially greater levels of prion protein in gingival
than in pulpal tissue of scrapie-infected
hamsters7.

There is little information on the precise infectivity of prion-infected
oral tissues. One study of scrapie-infected hamsters established that the
infectivity of pulpal tissue was 5.6 log LD50 while that of
gingival tissue was 72 log LD50. These were lower than the
infectivities of trigeminal ganglion and brain tissue.

Likelihood of transmission of prions during dental health care

First a word about experience with nosocomial transmission of non-prion
infectious agents during dentistry. Hepatitis B virus was at one time readily
transmitted during dental care, but contemporary infection control measures
have reduced this risk to almost
zero13. Although 6
patients probably acquired HIV as a consequence of care by an HIV-infected
dentist in the
USA14, lookback
studies of the patients of other HIV-infected dental staff have not disclosed
any patients infected with this virus as a result of dental
treatment15.
Dentists may be liable to hepatitis A virus infection, at least as evidenced
by HAV seroprevalence
studies16, although
they do not seem to be at risk of occupational acquisition of either hepatitis
C virus17 or
Transfusion Transmitted
Virus18. No dental
health care worker (DHCW) is believed to have been infected with HIV as a
consequence of occupational
injury15.

Clearly, these agents are much more easily activated than prions.
Epidemiological evidence offers some reassurance that prions are not likely to
be transmitted to DHCWs during dental treatment but the possibility cannot be
excluded.

Oral manifestations of prion disease

Oral manifestations of human transmissible spongiform encephalopathies are
dysphagia and dysarthria (due to pseudobulbar palsy), and in vCJD patients
there may be orofacial dysaesthesia or
paraesthesia19.
Loss of taste and smell has been reported in one patient with
vCJD20.

Possible routes of transmission of prions during dental care

Since prion protein of vCJD is likely to be in perioral lymphoid tissue,
and prions of scrapie can be transmitted via pulpal and gingival tissue, we
must assume that there is some risk, albeit small, of prion protein
transmission during dental care. The most likely means of transmission would
be via contaminated dental instruments; thus measures to reduce this risk are
essential in the dental surgical care of patients with known prion
disease.

GUIDELINES FOR THE DENTAL MANAGEMENT OF PATIENTS WITH PRION
DISEASE

Existing guidelines for the clinical management of patients with prion
disease do not address dental health care in any
detail21,22,23,
although this subject has been discussed
elsewhere24. In
general the suggested infection control procedures for the dental management
of patients with known prion disease are similar to those of all other
patients, with certain important modifications. At present oral tissues are
considered to be of low infectivity, so persons liable to iatrogenic CJD (i.e.
recipients of dura mater, corneal transplants and human pituitary hormones and
persons who have undergone neurosurgical procedures) are considered at low
risk of prion transmission, hence no additional infection control measures are
recommended other than those employed in universal cross-infection
control22.

Instruments must not be reused but discarded appropriately

The current UK guidance is that all health care instruments employed in the
treatment of a patient with known prion disease should be
discarded21,
22. Single-use
instruments are preferred, and these will come into increasing use for all
patients as new legislation comes into force.

Dental unit waterlines must not be activated

Dental unit waterlines can become contaminated with prions when the dental
handpiece is connected to the waterline. Thus, in view of the present
impossibility of inactivating prions, a sensible policy is to avoid the risk
of retraction of prions into the waterlines by instead using a coolant
provided by syringe.

Dental unit waterlines are a potential source of nosocomial infection.
Dental staff have an excess seroprevalence of influenza A and B viruses and
respiratory syncytial
virus24, this
possibly being due to the generation of
aerosols25 and the
development of biofilms within the lines. Dental staff also have an increased
seroprevalence of legionella, and titres may correlate with duration of dental
practice26.
Although the frequency of legionella seropositivity does not correlate with
rates of clinical
disease27, fatal
Legionella dumoffii in one dentist may have been due to acquisition
of infection from bacteria within the
waterline28. The
precise risk of acquisition by patients or dental health care staff of
infection from waterlines is not known, but since two immunosuppressed
patients developed nonfatal infection of Pseudomonas aeruginosa
derived from dental unit
waterlines29 there
is clearly a risk.

Biofilms of microorganisms derived from both the water source of the unit
and retracted oral fluids develop within 8 hours within
waterlines30. The
rapid biofilm formation reflects the low diameter to surface area of the
lines, the ease of adherence of bacteria to the hydrophobic polyurethane or
polyvinyl surface, the low rate of flow of water and the frequent long periods
of no flow within the
line31,
32.

Retraction of oral fluids into dental handpieces and the waterline is
common, indeed as much as 800 μL of fluid can pass into the
handpiece33.
Bacteria (e.g. Ps. aeruginosa) and viruses (e.g. HIV, hepatitis B,
herpes simplex, bacteriophage 174) have been found to be retracted into the
waterlines34.
Flushing even for 10-20 minutes does not remove the
biofilm35,36,37,38
(since the pressure at the tubing wall is almost
zero31) and
currently no antiretraction system, filtering
mechanism32, or
biocide has been reported to remove biofilms consistently from dental unit
waterlines.

Thus, since there is a risk of retraction of prions in oral fluids, it
would seem sensible not to activate waterlines when patients with known prion
disease require restorative dental care. There is little information on the
possible retraction of materials into the air lines of dental
units.

An independent suction and spittoon other than those of the dental
unit should be used

In view of the difficulties of disinfection, the suction system of the
dental unit cannot be used; instead a stand-alone suction unit should be used.
The reservoir of the suction unit should be disposable. Patients should
expectorate into a disposable bowl, not a spittoon, and this should be
discarded directly into the clinical waste bin for incineration.

CONCLUSIONS

Epidemiological evidence does not suggest that prion transmission as a
consequence of dental health care has occurred, but work in animals has
established that the oral tissues can become infected with prions and be a
potential source of infection in other animals. There is a need for research
to establish the potential susceptibility of oral tissues to infection by
prions of vCJD and bovine spongiform encephalopathy, and to determine the
exact infectivity of prion-containing oral tissues. At present the dental
instruments of patients with known prion disease should be discarded after
use. In view of the possible risk of contamination with prions due to
retraction of oral fluids it is advisable not to use the waterlines or suction
systems of dental units when treating patients with known prion disease.